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MAY MEDICINE 1 REVISION > CARDIOVASCULAR PATHOLOGY 3 > Flashcards

CARDIOVASCULAR PATHOLOGY 3 Flashcards

1
Q

What is hypertension ?

A

High blood pressure

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2
Q

What is blood pressure determined by ?

A

The cardiac output and the vascular resistance

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3
Q

What is the aim of hypertensive medication ?

A

To control cardiac output and vascular resistance

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4
Q

Name three vascular changes which can increase vascular resistance ?

A

Atheroma
Hypertrophy
Increased reactivity in resistance vessels

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5
Q

What is primary hypertension ?

A

Where the cause it not known

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6
Q

What is secondary hypertension ?

A

When the cause is known

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7
Q

What % of hypertension cases are secondary ?

A

10-20%

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8
Q

Can hypertension be cured?

A

Only secondary if the cause is removed

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9
Q

What conditions can cause secondary hypertension ?

A 
Renal disease 
Kidney disease 
Cortication of the aorta 
Pheochromocytoma 
Cushing syndrome 
Hyperthyroidism 
Recreational drugs 
Oral contraception's 
Corticosteroids
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10
Q

What is Pheochromocytoma ?

A

a small vascular tumour of the adrenal medulla, causing irregular secretion of adrenalin and noradrenaline

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11
Q

What is Cushing syndrome ?

A

Too much cortisol in the body

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12
Q

What features of hypertension suggest that it might be secondary ?

A
  • Severe
  • Resistant
  • Decaling
  • Malignant hypertension
  • Young people
  • No risk factors
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13
Q

Can hypertension be acute as well as chronic ?

A

Yes it can be a medical emergency

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14
Q

What is an example of a hypertensive medical emergency ?

A

Malignant hypertension

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15
Q

Describe Malignant hypertension

A

BP of 180/120 and evidence of acute organ damage

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16
Q

How is malignant hypertension treated ?

A

Lower BP by 10-20% in first hour
Lower to 160/100 in the next six hours.
This is done suing IV antihypertensives until target is met and then the patient is switched over to a oral medication

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17
Q

What can happen if you decrease BP too quickly ?

A

Increased chance of morbidity and mortality

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18
Q

When might a rapid reduction in BP be required ?

A

In ischemic stroke or aortic dissection

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19
Q

What is high BP which arises in pregnancy called?

A

gestational hypertension

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20
Q

What is high BP which was present before pregnancy called?

A

Chronic Hypertension

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21
Q

What is the second most common cause of maternal and foetal death ?

A

Gestational hypertension

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22
Q

What condition can result from high blood pressure in pregnancy ?

A

Pre-eclampsia.

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23
Q

Describe pre-eclampsia

A

A rapid rise in BP after 20 weeks gestation
BP > 140/90
Proteinuria > 300mg/24hrs

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24
Q

How is pre-eclampsia treated?

A

Antihypertensives

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25
Q

How is gestational hypertension and pre-eclampsia treated?

A

Antihypertensives and close monitoring

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26
Q

What are some risk factors for hypertension ?

A

Hypercholesteremia
Older age
Obesity

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27
Q

What are the signs and symptoms of hypertension ?

A 
High BP 
Headaches
SOB 
retinopathy or visual changes 
chest pain
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28
Q

What investigations are carried out to diagnose hypertension ?

A

20-30 BP readings using a ABPM or a HBPM
Assign risk calculator
Urinalysis to check for renal function
Serology to check for renin

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29
Q

What is a nocturnal dip?

A

When there is a reduction in blood pressure overnight.

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30
Q

What does a loss of nocturnal dip suggest ?

A

Organ damage i.e. Kidneys and heart

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31
Q

What is white coat hypertension ?

A

when a patient has a high BP at the doctors because of stress but a normal BP the rest of the time

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32
Q

What is masked hypertension ?

A

when a patient has a normal BP at the doctors but a high BP the rest of the time

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33
Q

What does the assign risk calculator do ?

A

used to work out the risk of a patient suffering a major cardiac event in the next 10 years.

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34
Q

What is stage 1 hypertension ?

A

ABPM daytime average Stage 1 hypertension = BP ≥ 135/85

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35
Q

What is stage 2 hypertension ?

A

Stage 2 hypertension = BP ≥ 140/90

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36
Q

What is stage 3 hypertension ?

A

Stage 3 hypertension = BP ≥ 180/120

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37
Q

What are some non-pharmacological treatments for hypertension ?

A

exercise, reduced salt intake, good diet, limited alcohol, smoking cessation

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38
Q

When should phrenological treatments be started ?

A

CVD risk is ≥10% over the next 10 years

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39
Q

What is the aim of treatment ?

A

get BP <135/85 or <145/85 in > 80 year olds

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40
Q

What is the antihypertensive of choice for a person of African/Carrabin family origin ?

A

Thiazide a diuretic

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41
Q

What is the antihypertensive of choice for a person over 55 yo or of child bearing capacity ?

A

A CCB

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42
Q

What is the antihypertensive of choice for a person under 55 yo ?

A

ACEI

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43
Q

How is stage 1 hypertension treated ?

A

antihypertensive of choice in those over 80 or those with target organ damage, establish CVS disease, renal disease or a 10% risk of a major CVS event in the next 10 years

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44
Q

How is stage 2 hypertension treated ?

A

Stage 2 hypertension is treated with an antihypertensive for all.

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45
Q

Describe how hypertensive treatment can be escalated ?

A

If treatment doesn’t work then thiazide can be added to a CCB or ACEI/ARB. If that still doesn’t work then you can consider using CCB, ACEI and a diuretic which is a very powerful combination.

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46
Q

Name two common ACEIs

A

Ramipril and perindopril

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47
Q

How doe ACEIs work ?

A

They Inhibit the actions of ACE (lowering BP). ACEIs can have ADRs with NSAIDs causing acute renal failure.

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48
Q

What are some contraindications of ACEIS?

A

Renal impairment,

Fertile females,

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49
Q

What is the made side effect of an ACEI?

A

Main side effect is a dry cough

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50
Q

What are ARBs?

A

They can be used instead of an ACEI where a patient cant have an ACEI

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51
Q

Name a few ARBs

A

losartan, valsartan and candesartan

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52
Q

Describe ARBs

A

competitively block angiotensin II at the angiotensin AT1 receptors. ARBs are similar to ACEIs but don’t produce a cough

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53
Q

Names some common CCBs

A

amlodipine or felodipine

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54
Q

How do CCBs work ?

A

Calcium allows myocyte contraction in blood vessels and heart. CCBs bind to L type channels in the myocytes preventing calcium from acting of the myocytes and therefore reducing contraction, decreasing HR and causing vasodilation

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55
Q

Common side effects of CCBs

A

cause flushing, headaches, ankle oedema, indigestion etc especially in women

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56
Q

Contraindications of CCBs

A

MI, heart failure, bradycardia

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57
Q

Name 1 example of a thiazide

A

indapamide

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58
Q

How does thiazide work ?

A

They enhance urinary excretion of sodium but they may take a number of week before the full effects are felt.

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59
Q

Complications of a thiazide

A

Gout and ED

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60
Q

What is Atheroma/Atherosclerosis ?

A

an elevated lesion or plaque on the intima or a large or medium sized artery

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61
Q

Where do Atheroma/Atherosclerosis usually form ?

A

at the branching or bifurcation points where there is turbulent flow

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62
Q

What does atheroma do to the vessel diameter ?

A

Reduces it

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63
Q

Describe the process by which an atheroma forms

A

In arteries endothelial cells become injured or dysfunction. This allow LDL from the plasma to move into the tunica intima of the blood vessels. The presence of LDL in the intima causes endothelial cells to release molecules which oxidise the LDL. Oxidised LDL causes the endothelial cells express leukocytes adhesion molecules on there surface. Monocytes and T-helper cells bind to the endothelial receptors and move into the intima. Monocytes become macrophages and engulf the oxidised LDL and become ‘foam cells’. Foam cells have a number of roles including stimulating the migration and proliferation of smooth muscle cells from the tunica media into the tunica intima. Smooth muscle cells stimulate the formation of collagen. When a foam cell dies it released its lipid content. This combination of cells and debris result in inflammation. This is known as the atheroma plaque.

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64
Q

What is a fatty streak ?

A

The first stage of atherosclerosis where there is a build up of lipid-laden macrophages in the intima. These can develop in children

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65
Q

Describe the cap of an atheromatous plaque

A

Over time fatty streaks develop into atheroma plaques which have a central lipid core and a fibrosis cap. The cap contains the collagen and inflammatory cells. In late stages the cap can become calcified and the plaques will merge to cover large areas

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66
Q

Describe the core of an atheromatous plaque

A

The lipid core is where the debris is and this is very thrombogenic

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67
Q

How do plaques grow ?

A

Plaques can also grow by forming repeated microthrombi in areas of endothelial cell loss.

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68
Q

Name two things which can happen to an atheroma ?

A
  • A thrombus can develop on it

- It can rupture

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69
Q

What are some risk factors of Atheroma ?

A 
Hypercholesterolemia 
Hypertension 
Obesity 
old age 
Diabetes
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70
Q

What are the signs and symptoms of atheroma ?

A

It is usually asymptomatic until it results in an acute condition

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71
Q

How is atheroma treated ?

A

Prevention, cholesterol lowering drugs. Sometimes surgery.

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72
Q

What is the prognosis of atheroma ?

A

Thrombosis or ruptured plaque can embolise and cause ischemic stroke or ischemic heart disease

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73
Q

What is a another name for Ischemic heart disease ?

A

coronary heart disease

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74
Q

How many coronary heart disease are there ?

A

4

75
Q

What are the two causes of coronary heart disease ?

A

. The main cause of these conditions is a blocked artery (usually a result of atheroma) however it can also be caused by a mismatch between supply and demand

76
Q

What is ischemia ?

A

reduction in blood flow through a vessels

77
Q

What is hypoxia ?

A

lack of oxygen to the tissue supplied by that vessel

78
Q

What is infarction ?

A

serious coronary artery disease it can result in the death

79
Q

What is type 1 MI ?

A

MI caused by blockage in the artery

80
Q

What is type 2 MI ?

A

myocardial infarction is caused by a mismatch between supply and demand.

81
Q

What is the basic timescale of MI ?

A

As a basic timeline of cellular damage, when occlusion of a vessel occurs cells change to anaerobic metabolism and ATP depletion occurs within the first few seconds. After 2 mins there is loss of myocardial contractility. After 5 mins there is a change to the ultrastructure. After 20-30 mins damage becomes irreversible. After 20-40 mins necrosis starts and after 1 hours there is damage to the microvasculature.

82
Q

What are the signs and symptoms of coronary artery disease ?

A

Chest tightness, which is often described as a weight rather than a pain. This chest discomfort often radiates down the arm and up into the jaw.
Dyspnoea,
sweating,
nausea,
looking very sick are also key signs and symptoms.

83
Q

What % of a vessel has to be blocked in order to have angina symptoms ?

A

70%

84
Q

What are risk factors for ischemic heart disease ?

A

male, old age, heart disease, high cholesterol, smoking, family history, diabetes.

85
Q

What is stable angina ?

A

Generally the presence of an atheroma plaque in a coronary artery can be thought to cause it. When at rest the blockage isn’t sufficient to prevent adequate blood supply to myocardium however when exercising the blockage prevents the increased oxygen demand from being met. Therefore a patient will experience symptoms only when exercising

86
Q

What investigations should be done for stable angina ?

A

When diagnosing a patient with stable angina an ECG should be carried out. This will be normal however it is important to do in order to rule out a more serious coronary artery disease. A coronary angiogram and a full blood test should also be performed. The severity of stable angina can be measured using the CCS score (see image).

87
Q

Describe what troponin is

A

Blood tests are used to test for troponin which is a protein found in the sarcomere of cardiac cells. This protein is released when the cell dies and to if there has been any MI then there will be elevated troponin. T

88
Q

What are the names of other biomarkers in the blood showing MI

A

CK-MB or myoglobin.

89
Q

What is the treatment for stable angina ?

A

The patient should be given GTN to take when experiencing symptoms.
The patient should also be given a beta blockers (or a CCB if cant take a BB) in order to prevent attacks from happening. If this is not sufficient then a long-acting nitrate can be added in.
CABG and PCI surgery can also be carried out if the patient does not respond to treatment or if CVD risk is high enough.
On discharge long term medication should be started to help prevent ACS or stroke. These include a low dose aspirin, statins or an ACEIs.

90
Q

What is the CCS classification ?

A

-

91
Q

What is unstable angina ?

A

Generally this is caused when a thrombus on the plaques or an atheroma plaque which has ruptured embolises to the coronary arteries. This causes partial occlusion of the vessel and ischemia of heart tissue. This ischemia occurs when at rest

92
Q

Investigations for unstable angina include

A

Again an ECG, coronary angiogram and blood tests are carried out. The ECG will usually no normal however it is good to rule out other causes

93
Q

Treatment for unstable angina includes ?

A

Dual anti-platelet therapy should be started and this will be continues indefinitely.
A prophylaxis fondaparinux is also started (unless a patient is about to go for a coronary angiogram). This drug helps to prevent further thromboembolism in the future.
CABG or PCI surgery is also recommended and
statins should be given in cholesterol is > 3.5 mmol/l.

94
Q

What is a NSTEMI ?

A

Generally this is caused when a thrombus on the plaques or an atheroma plaque which has ruptured embolises to the coronary arteries. This causes partial occlusion of the vessel and ischemia and infarction of heart tissue.

95
Q

Investigations for NSTEMI

A

An ECG should be carried out and then treatment should be started. After a patient has been stabilised other tests can be carried out. A blood test to check for troponin is very important. CXR, Echocardiogram and coronary angiogram are also usually done.

96
Q

What will an ECG show in a NSTEMI ?

A

The ECG may have T wave inversion, slight ST depression and after three days the absence of a Q wave.

97
Q

Treatment for NSTEMI

A

Dual anti-platelet therapy should be started and this will be continues indefinitely. A prophylaxis fondaparinux is also started (unless a patient is about to go for a coronary angiogram). This drug helps to prevent further thromboembolism in the future. CABG or PCI surgery is also recommended and statins should be given in cholesterol is > 3.5 mmol/l.

98
Q

What is STEMI ?

A

Generally this caused when a thrombus on the plaques or an atheroma plaque which has ruptured embolises to the coronary arteries. This causes complete occlusion of the vessel and ischemia and infarction of heart tissue

99
Q

Investigations for STEMI

A

An ECG should be carried out and then treatment should be started. After a patient has been stabilised other tests can be carried out. A blood test to check for troponin is very important. CXR, Echocardiogram and coronary angiogram are also usually done.

100
Q

What will an ECG show in a STEMI ?

A

An ECG will show ST elevation or if the MI is in the posterior of the patient then possible ST depression.

101
Q

Treatment for STEMI

A

A PCI operation is the preferred treatment however if a patient cant have a PCI or cant get to a Cath lab in less then 2 hours then thrombolysis is given. Dual anti-platelet therapy should be started and this will be continues indefinitely. A prophylaxis fondaparinux is also started (unless a patient is about to go for a coronary angiogram). This drug helps to prevent further thromboembolism in the future. CABG or PCI surgery is also recommended and statins should be given in cholesterol is > 3.5 mmol/l.

102
Q

what is considered a ACS ?

A

Unstable angina, NSTEMI and STEMI

103
Q

How is MI diagnosed ?

A

In order to diagnosis a MI you must have evidence of cell death (i.e., elevated troponin) and one of the following: Symptoms of ischemia, new ECG changes, evidence of coronary problem on coronary angiogram or autopsy, or evidence of new cardiac damage on another test.

104
Q

What two things should also be offered as well as pharmacological treatment ?

A
  • General management

- Non-pharmacological

105
Q

What is dual antiplatelet therapy ?

A

Dual antiplatelet therapy should be given. This is the combination of aspirin (300mg loading dose, then 75-150mg each day thereafter. Patients should be on long-term aspirin therapy) and ticagrelor (which is a P2Y12 ADP receptor antagonists, loading dose is 180mg and then 90mg per day). Patients should receive this dual antiplatelet therapy for at least six months. A long term statin, beta blocker and ACEI should also be started before discharge from hospital. Other P2Y12 ADP drugs which are less common are clopidogrel a prodrug (300 mg loading dose, then 75 mg od) and prasugrel (60 mg loading dose then 10 mg od) which is fast acting.

106
Q

What is a coronary angiogram ?

A

Coronary angiogram is minimally invasive procedure used to used to view the coronary arteries. PCI or angioplasty is when balloons and stents are put into the coronary arteries during a coronary angiogram to dilate the blood vessels and then keep them open in the future. Risks of PCI include bleeding from atrial access site (Normally you go into though the radial artery), MI, coronary perforation, emergency CABG, stoke or the dye can affect the kidneys causing contract nephropathy. CABG or bypass surgery is performed when the blockage is very severe.

107
Q

What is thrombolysis ?

A

Thrombolysis (mostly serine proteases which convert plasminogen to plasmin which then breaks down clots) is most effective in the first two hours. This drug can be given by ambulances. Fibrinolysis can be offered within the first 12 hours. Thrombolysis cannot be given if the patient has an intercranial haemorrhage. Thrombolysis carried a risk of bleeding, for this reason don’t give to a patient who has had a recent stroke or ever had a previous intracranial bleed. Known structural cerebral vascular lesion, intracranial neoplasm malignancy, ischemic stoke within last 3 months, recent surgery or warfarin or sever hypertension, suspected aortic dissection, active blood or bleeding diathesis etc. If the patient is scheduled for PCI then prasugrel can be added to aspirin.

108
Q

What are the main risk factors for stroke ?

A

hypertension (associated with lunar strokes. Risk increases dramatically when BP >160), Smoking (2x risk of ischemic stroke and x3 risk of haemorrhage stroke), diabetes, obesity, family history, high cholesterol, personal cardiac history.

109
Q

If you smoke how much more likely are you to have an ischemic stoke?

A

2x

110
Q

If you smoke how much more likely are you to have an haemorrhagic stoke?

A

3x

111
Q

What do stroke symptoms depend on ?

A

location

112
Q

What is a TACS?

A

Total anterior circulation stoke which have a high mortality and low rate of recurrence

113
Q

What are PACS ?

A

partial anterior circulation stroke higher rate of recurrence but lower mortality

114
Q

What are LACS?

A

Lunar stroke low mortality and low recurrence

115
Q

What are POCS?

A

posterior circulation stoke higher rate of recurrence but lower mortality

116
Q

Examples of stroke sympoms

A

Sudden numbness or weakness in the face, arm, or leg, especially on one side of the body.
Sudden confusion, trouble speaking, or difficulty understanding speech.
Sudden trouble seeing in one or both eyes.
Sudden trouble walking, dizziness, loss of balance, or lack of coordination.
Remember FAST !!!!!

117
Q

Examples of posterior stroke symptoms

A

Vertigo, imbalance, slurred speech.

118
Q

Examples of anterior stroke

A

loss of sensation, loss of sight, Speech problems.

119
Q

What is the treatment for stroke ?

A

Get patients to a stroke unit as fast as possible and get them mobilised by nurses.
Give Aspirin.
Restore blood supply, prevent ischemic damage. Alteplase is a thrombolysis which should be given within the first 4.5 hours. Treatment after 4.5 hours will have no benefit. It carried a risk of bleeding.
Clot retrieval procedure and carotid endarterectomy can also be carried out. antiplatelets, stains and blood pressure management anticoagulants

120
Q

Investigations for stroke

A

Get a plane CT. Perfusion CT, DWI or PWI or CT angiogram etc are helpful but often can’t be done fast enough.

121
Q

What is a stroke ?

A

a neurological deficit (Loss of function of some part of the body) which has had sudden onset and has lasted more than 24hours and has vascular origin (Caused by a blockage or rupture to a blood vessel in the brain).

122
Q

What is a TIA

A

a transient ischaemic attack where symptoms last for less than 24 hours

123
Q

Describe ischemic strokes

A

85-90% of strokes are ischemic strokes where a vessel is blocked and results in infarction of brain tissue. If an Atheroma ruptures, it can embolise to the brain and cause stroke. The ruptured plaques can often be part of a large artery disease such as carotid stenosis or carotid dissection. Ischemic stroke can also be caused by disease of a vessel wall or abnormal blood properties (i.e. too many RBCs). Sometimes it is an embolism but not from a ruptured plaque. This is the case in atrial fibrillation where clots can form and travels from the heart to the brain. In a stroke there is an area surrounding the dead tissue called a penumbra. These cells are not yet but are not receiving the oxygen that they need. In a lunar stroke there is a blockage of the small vessels of the brain which is normally caused by hypertension or vessel wall thickening. Although it only affects a small area because the fibres are close together it often does a lot of damage.

124
Q

Describe haemorrhagic strokes

A

10-15% of strokes are caused by a haemorrhage. A haemorrhage can be caused by hypertension, amyloid, excess alcohol and hypercholesterolaemia. This results in an inflammatory response which further damages the brain. This kind of stroke has the highest rate of death in 30 days after stoke.

125
Q

What are some secondary complications of a stroke which cause further tissue damage ?

A

Haemorrhage,
oedema,
lactic acid build up which disrupts acid-base balance (caused when cells go into anaerobic respiration in hypoxia).

126
Q

What is an arrhythmia ?

A

a deviation from the normal rhythm of the heart

127
Q

What is used to diagnose an arrhythmia ?

A

an ECG

128
Q

Name an arrhythmia which is not dangerous to have ?

A

ectopic beat

129
Q

Describe the treatment for ectopic beats ?

A

Normally nothing. If they are particularly bothersome for the patient Beta blockers can be given.

130
Q

Draw the diagram which classifies arrhythmias

A

-

131
Q

describe 1st degree block

A

1st Degree block is where there is a increased time between the p wave and the QRS complex.

132
Q

Describe 2nd degree block

A

2nd Degree block is where there is an increasing time between the p wave and the QRS complex. There are two types. Mobitz type 1 is where there is progressive PR interval until the sixth P wave fails. Here P-P interval remains constant. In Mobitz type 2 the 2nd and 8th P waves are not conducted and P-P interval remains constant.

133
Q

Describe 3rd degree block

A

3rd Degree block is where there is no relationship between the P wave and the QRS complex. Note that the P waves are still regular.

134
Q

describe atrial flutter

A

Atrial flutter is where there are depolarisations which are occurring too quickly. Common symptoms include palpitations, dyspnoea and dizziness. It has a good prognosis and often there is no treatment. If it is occurring very often then catheter ablation can be considered.

135
Q

describe atrial fibrillation

A

Atrial fibrillation is where the p wave is missing. This is especially clear on V1. There will be an irregular pulse. Common symptoms are palpitations, dyspnoea, chest pain and fatigue though there may be no symptoms. Treatment is important as this is often the first sign of a thromboembolism. Investigations include a 24 hours ECG and a blood test for thyroid function. An echocardiogram should also be done.

136
Q

describe ventricular tachycardia

A

Ventricular tachycardia are fast rhythmic disturbances that arise from within the ventricles. They cause palpitations, dyspnoea etc. Treatment is to treat the cause which is often an underlying heart disease

137
Q

describe ventricular fibrillation

A

Ventricular fibrillation is the totally uncoordinated depolarisation and contracting of the heart. Here a defibrillator is required.

138
Q

What are three ways in which arrhythmias can be treated ?

A

Antiarrhythmics, anticoagulants and pacemakers.

139
Q

What method can be used to classify antiarrhythmics ?

A

Vaughan-William’s classification system.

140
Q

describe class 1 Antiarrhythmics

A

Fast sodium channel blockers and membrane stabilisers
They reduce the amplitude and conduction velocity of AP
They can be divided into 1A moderate, 1B weak and 1C strong.
Flecainide is the most commonly used and it is a IC

141
Q

describe class 2 Antiarrhythmics

A

Beta blockers which prevent sympathetic stimulation of the heart, slowing SA discharge and AV conduction.
First line atrial fibrillation treatment
Atenolol and bisoprolol

142
Q

describe class 3antiarrhythmics

A

increase AP duration and increase repolarisation
Used to treat ventricular tachycardia, ventricular fibrillation atrial fibrillation and atrial flutter which have not responded to other drugs
Amiodarone. It does however have many drug to drug interactions including with digoxin and many side effects i.e. Pulmonary fibrosis

143
Q

describe class 4 antiarrhythmics

A

Calcium channel blockers which bind to l type Ca channels and slow muscle contraction
Diltiazem and verapamil

144
Q

describe class 5 antiarrhythmics

A

Other drugs

145
Q

Describe digoxin

A

inhibits the Na/K pump. It can cause toxicity and therefore should be monitored closely.
Signs of toxicity include nauseous, vomiting, bradycardia, reverse tick appearance of the ST segment.
Treatment for toxicity is to stop digoxin and give digibind which binds to digoxin in the body and helps it to be excreted in the urine.

146
Q

When should anticoagulation be given ?

A

In atrial fibrillation and to anyone with a Chadsvac score of 2 or above

147
Q

What is warfarin ?

A 
Anticoagulant 
Vitamin K antagonist
Very narrow therapeutic range  
Often causes bleeding
Cant be given in pregnancy
148
Q

What can be sued to estimate the risk of bleeding when giving warfarin ?

A

HASBLED

149
Q

When might a pacemaker be temporarily fitted?

A
  • An abnormally slow heart rate
  • An abnormally fast heart rate
  • Heart block
150
Q

When might a pacemaker be permanently fitted?

A
  • profound 2/3 degree heart block

- Cardiac arrest

151
Q

What are the three types of valvular disease?

A

Stenosis
Regurgitation
Infection

152
Q

What is stenosis ?

A

Valvular disease can be stenosis where there is thickening, calcification of valves which obstructs normal blood flow

153
Q

What is regurgitation ?

A

Valvular disease can also be regurgitation (also called incompetence)( where the valve function is lost and it fails to prevent reflex of blood

154
Q

What is infective valvular disease ?

A

Valvular disease can also be where infective or thrombotic nodules develop on the valves and impair the function.

155
Q

How many cusps does the mitral valve have ?

A

2

156
Q

How many cusps does the other valve have ?

A

3

157
Q

Will a disease of the left ventricular affect the mitral valve ?

A

yes

158
Q

What is mitral stenosis ?

A

Mitral stenosis is where there is narrowing of the valve (orifice < 2cm).

159
Q

What causes mitral stenosis ?

A

rheumatic heart disease, it can be congenital or the result of a systemic condition

160
Q

What does mitral stenosis do ?

A

Mitral stenosis increases the pressure gradient between atrium and ventricle.
It can cause a backlog of blood and eventually result in pulmonary hypertension and dilation of the right heart.

161
Q

What does the severity of mitral stenosis depend on ?

A

The severity of mitral stenosis depends on trans-valvular (across the valve) pressure gradient and trans valvular flow rate

162
Q

How will mitral stenosis present ?

A

. It will present with SOB, haemoptysis, symmetric embolization, chest pain and hoarseness, infective endocarditis, raised JVP, trapping apex beat and diastolic thrill. There may also be a diastolic murmur.

163
Q

What investigations are used to look into mitral stenosis?

A

Investigations include an ECG and a occasionally a cardiac catheterisation. CXRs may show left atrial enlargement

164
Q

How is mitral stenosis diagnosed ?

A

Diagnosis is done from echocardiogram where there will be thickening and scarring of the cusps and fusion of the commissures (openings).

165
Q

How is mitral stenosis treated ?

A

It is treated with diuretics and restrictions of NA intake. Valvotomy surgery can also be done.

166
Q

What causes mitral regurgitation ?

A

Mitral regurgitation is due to rheumatic heart disease, mitral valve prolapse and Infectious endocarditis

167
Q

Signs and symptoms of mitral regurgitation ?

A

Acute: breathless, have pulmonary oedema and cardiogenic shock.
Chronic: with fatigue, right heart failure, SOB and palpitations due to the development of AF

168
Q

Investigations for mitral regurgitation ?

A

Echo
ECG which will show LA enlargement
CXR to show cardiomegaly

169
Q

Treatment for mitral regurgitation

A

Acute: Vulvectomy with 12 hours
Chronic: Valvectomy.

170
Q

What is aortic stenosis caused by ?

A

old age or rheumatic disease or it can be congenital (sometimes patients are born with a bicuspid valve which goes on to cause AS).

171
Q

What are the two types of aortic stenosis?

A

rheumatic

degenerative

172
Q

describe rheumatic aortic stenosis

A

AS can be rheumatic where there is fusion of the commissures and retraction and stiffening or the cusps.

173
Q

describe degenerative aortic stenosis

A

it si much like atherosclerosis, a slow inflammatory process resulting in thickening and calcification of the cusps

174
Q

What can be a consequence of aortic stenosis?

A

MI

LV failure

175
Q

Signs and symptoms

A

Aortic stenosis has a very long asymptomatic phase however symptoms do develop and when they do the life expectancy for the patient fall rapidly. Typical symptoms include chest pain, syncope/dizziness, breathlessness on exertion and heart failure. On examination there will be a prominent JVP if heart failure is present and a vigorous and sustained apex beat. An ECG is used to show LV hypertrophy.

176
Q

Investigations for aortic stenosis

A

An Echocardiogram

177
Q

Treatment for aortic stenosis

A

Treatment is only given to those who then develop heart failure. In that case intervention treatments such as aortic valve repair or replacement can be carried out. It is found in calcific aortic valve disease.

178
Q

What is aortic regurgitation ?

A

Aortic regurgitation can be caused by the aorta where the aorta is dilated or there is connective tissue disorder

179
Q

Can regurgitations be acute and chronic ?

A

yes

180
Q

Describe chronic aortic regurgitation

A

a long asymptomatic phase, and then develops to present exertional breathlessness.

181
Q

Describe acute aortic regurgitation

A

. Acute AR is poorly tolerated as wall tension cannot acutely adapt and so this is an medical emergency. On clinical examination there will be a large volume and collapsing pulse.

182
Q

Investigations for aortic regurgitation

A

Echo

ECG ST/T changes and left axis deviation

183
Q

How is aortic regurgitation treated ?

A

vasodilatory therapy is used as it is shown to delay the timing for surgical intervention. Interventional treatment increase aortic valve replacement or repair.

MAY MEDICINE 1 REVISION (23 decks)

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